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81.
Yamashita Yugo Amano Hidewo Morimoto Takeshi Kadota Kazushige Hata Reo Matsushita Kazuki Osakada Kohei Sano Arata Takase Toru Hiramori Seiichi Kim Kitae Oi Maki Akao Masaharu Kobayashi Yohei Toyofuku Mamoru Inoko Moriaki Tada Tomohisa Chen Po-Min Murata Koichiro Tsuyuki Yoshiaki Nishimoto Yuji Sasa Tomoki Sakamoto Jiro Kinoshita Minako Togi Kiyonori Mabuchi Hiroshi Takabayashi Kensuke Kato Takao Ono Koh Kimura Takeshi 《Journal of thrombosis and thrombolysis》2022,53(1):182-190
Journal of Thrombosis and Thrombolysis - Prolonged anticoagulation therapy is recommended for patients with intermediate-risk for recurrence of venous thromboembolism (VTE). The current study aimed... 相似文献
82.
Assignment of CSF-1 to 5q33.1: evidence for clustering of genes regulating hematopoiesis and for their involvement in the deletion of the long arm of chromosome 5 in myeloid disorders. 总被引:9,自引:3,他引:9 下载免费PDF全文
M J Pettenati M M Le Beau R S Lemons E A Shima E S Kawasaki R A Larson C J Sherr M O Diaz J D Rowley 《Proceedings of the National Academy of Sciences of the United States of America》1987,84(9):2970-2974
The CSF-1 gene encodes a hematopoietic colony-stimulating factor (CSF) that promotes growth, differentiation, and survival of mononuclear phagocytes. By using somatic cell hybrids and in situ hybridization, we localized this gene to human chromosome 5 at bands q31 to q35, a chromosomal region that is frequently deleted [del(5q)] in patients with myeloid disorders. By in situ hybridization, the CSF-1 gene was found to be deleted in the 5q- chromosome of a patient with refractory anemia who had a del(5)(q15q33.3) and in that of a second patient with acute nonlymphocytic leukemia de novo who had a similar distal breakpoint [del(5)(q13q33.3)]. The gene was present in the deleted chromosome of a third patient, with therapy-related acute nonlymphocytic leukemia, who had a more proximal breakpoint in band q33 [del(5)(q22q33.1)]. Hybridization of the CSF-1 probe to metaphase cells of a fourth patient, with acute nonlymphocytic leukemia de novo, who had a rearrangement of chromosomes 5 and 21 [ins(21;5)(q22;q31.3q33.1)] resulted in labeling of the breakpoint junctions of both rearranged chromosomes; this suggested that CSF-1 is located at 5q33.1. Thus, a small segment of chromosome 5 contains GM-CSF (the gene encoding the granulocyte-macrophage CSF), CSF-1, and FMS, which encodes the CSF-1 receptor, in that order from the centromere; this cluster of genes may be involved in the altered hematopoiesis associated with a deletion of 5q. 相似文献
83.
Protein C activation in NIDDM patients 总被引:6,自引:0,他引:6
E. C. Gabazza H. Takeya H. Deguchi Y. Sumida O. Taguchi K. Murata K. Nakatani Y. Yano M. Mohri M. Sata T. Shima J. Nishioka K. Suzuki 《Diabetologia》1996,39(12):1455-1461
Summary Enhanced activation of the clotting system has been recently implicated in the pathogenesis of vascular complications in
patients with diabetes mellitus. Abnormalities of the anticoagulant system may constitute a potential trigger factor for the
haemostatic activation observed in diabetic subjects. The current study aimed to evaluate anticoagulant activity in diabetic
patients by assessing the plasma levels of activated protein C-protein C inhibitor complex; and by measuring the anticoagulant
response to exogenous thrombomodulin. This study comprised 61 patients (34 men, 27 women) with non-insulin-dependent diabetes
mellitus (NIDDM) of whom 22 showed microalbuminuria and 39 normoalbuminuria. Data obtained in 31 non-obese and non-diabetic
subjects were available for comparison. The plasma levels of fibrinogen (p < 0.02), prothrombin fragment 1 + 2 (p < 0.05), fibrin monomer (p < 0.0001), protein C antigen (p < 0.005), total protein S antigen (p < 0.02), soluble thrombomodulin (p < 0.005) and soluble E-selectin (p < 0.005) were significantly higher in diabetic patients than in healthy subjects. The plasma level of activated protein C-protein
C inhibitor complex (7.4 ± 3.8 vs 3.0 ± 0.4 pmol/l) was significantly higher (p < 0.0001) and the anticoagulant response to exogenous thrombomodulin (23.4 ± 2.6 vs 35.3 ± 3.0 ng/ml) was markedly lower
(p = 0.005) in all diabetic patients than in healthy subjects. Cases with microalbuminuria presented low plasma levels of activated
protein C-protein C inhibitor complex (5.5 ± 0.6 vs 8.6 ± 0.7 pmol/l, p < 0.05) and significantly decreased values of the anticoagulant response to exogenous thrombomodulin (16.5 ± 2.9 vs 23.4
± 2.6 %, p = 0.03) as compared to those with normoalbuminuria. The present study suggests that the hyper-coagulable state in NIDDM is
associated with an increased activation of protein C but with a poor plasma reactivity to the anticoagulant effect of thrombomodulin.
[Diabetologia (1996) 39: 1455–1461]
Received: 27 February 1996 and in revised form: 3 June 1996 相似文献
84.
Marked increases of two kinds of two-exon-skipped albumin mRNAs with aging and their further increase by treatment with 3''-methyl-4-dimethylaminoazobenzene in Nagase analbuminemic rats. 总被引:2,自引:1,他引:2 下载免费PDF全文
T Kaneko H Shima H Esumi M Ochiai S Nagase T Sugimura M Nagao 《Proceedings of the National Academy of Sciences of the United States of America》1991,88(7):2707-2711
Nagase analbuminemic rats (NARs) have a 7-base-pair deletion at the 5' splice site of the HI intron of the albumin gene. The level of immunohistochemically albumin-positive hepatocytes is about 1 per 10(5) cells in neonatal NARs, increases with age, and further increases with chronic oral treatment with 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB). The mechanisms involved in the increase in albumin-positive hepatocytes during aging of NARs and their treatment with 3'-MeDAB were analyzed. NARs were found to have four species of albumin mRNA: intact mRNA and those lacking the regions corresponding to exon H, exon G-H, and exon H-I. In 4-week-old NARs, the level of intact albumin mRNA was about 1/4000 of that in normal rats and mRNA lacking the exon H sequence was the major species. In aged and 3'-MeDAB-treated aged NARs, all four species of mRNA increased and the relative proportion of mRNAs lacking two exon sequences to mRNAs lacking one exon sequence was greatly increased, suggesting that aging is associated with changes of the splicing pattern and that 3'-MeDAB treatment enhanced these changes. In aged NARs and 3'-MeDAB-treated aged NARs, there was an increase in the amount of aberrant 60-kDa albumin. The 60-kDa protein could be a translation product of mRNAs lacking two exons, the amount of which increases in aged NARs and 3'-MeDAB-treated NARs. 相似文献
85.
J. Fu H. Ikegami Y. Kawaguchi T. Fujisawa Y. Kawabata Y. Hamada H. Ueda M. Shintani K. Nojima N. Babaya Q.-J. Shen Y. Uchigata T. Urakami Y. Omori K. Shima T. Ogihara 《Diabetologia》1998,41(2):228-232
Summary An insulin-dependent diabetes mellitus (IDDM)-susceptibility gene (IDDM13) has recently been mapped to a region of distal chromosome 2q, which is syntenic to the region of mouse chromosome 1 containing
a murine susceptibility gene for IDDM, Idd5. To determine the contribution of this region to IDDM disease susceptibility further and to narrow the region for positional
cloning of susceptibility genes, we have studied the association of distal chromosome 2q with IDDM in the genetically distinct
Japanese population. A 137 mobility unit (mu) allele at D2S137 locus was significantly associated with IDDM (odds ratio 1.92, p = 0.0016). Other markers, D2S301 and D2S143, located in the same region were not associated with IDDM, indicating that IDDM13 is in linkage disequilibrium with D2S137, but not with D2S301 or D2S143. The association of D2S137 with IDDM was observed in patients lacking one of two high risk HLA alleles, DQB1
*
0303 and DQB1
*
0401, but not in patients with either of these alleles. The frequency of high risk HLA alleles was significantly lower in patients
with the susceptible allele at D2S137, suggesting that IDDM13 contributes to IDDM susceptibility in subjects without high risk genotypes at IDDM1. Demonstration of allelic association of D2S137 with IDDM localizes IDDM13 in the close vicinity (< 2 centiMorgans) of D2S137, greatly facilitating fine structure mapping and positional cloning of IDDM13. [Diabetologia (1998) 41: 228–232]
Received: 27 March 1997 and in revised form: 3 October 1997 相似文献
86.
Kimura M Higashi Y Hara K Noma K Sasaki S Nakagawa K Goto C Oshima T Yoshizumi M Chayama K 《Hypertension》2003,41(5):1106-1110
Smoking is associated with endothelial dysfunction. The purpose of this study was to determine the effect of sildenafil, an inhibitor of phosphodiesterase type 5 (PDE5), on endothelial function in smokers. We evaluated the forearm blood flow (FBF) responses to acetylcholine (ACh), an endothelium-dependent vasodilator, and to sodium nitroprusside (SNP), an endothelium-independent vasodilator, before and after oral sildenafil administration (100 mg) with a strain-gauge plethysmograph in 10 young healthy male smokers and 10 young healthy male nonsmokers. FBF response to ACh was lower in smokers than in nonsmokers. The vasodilatory effects of SNP were similar in both groups. Sildenafil increased the FBF response to ACh from 9.3+/-2.0 to 12.5+/-3.5 mL/min per 100 mL tissue in smokers and from 12.6+/-5.6 to 19.6+/-8.4 mL/min per 100 mL tissue in nonsmokers, and it increased the response to SNP from 13.3+/-3.9 to 15.1+/-4.3 mL/min per 100 mL tissue in smokers and from 14.8+/-5.2 to 18.4+/-6.0 mL/min/100 mL tissue in nonsmokers (P<0.05 for all). The ratio of maximal ACh-stimulated FBF expressed as a ratio of maximal SNP-stimulated FBF significantly increased after administration of sildenafil in both groups. Infusion of NG-monomethyl-L-arginine, a nitric oxide synthase inhibitor, abolished sildenafil-induced augmentation of the FBF response to ACh in both groups. The findings suggest that endothelial function is impaired in smokers compared with that in nonsmokers, that inhibition of PDE5 by sildenafil significantly increases nitric oxide-mediated vasodilation, and that the activities of PDE5 in smokers and nonsmokers may be similar. 相似文献
87.
Azuma A Matsuo A Nakamura T Kawasaki T Yamamoto K Hyogo M Hirata A Hirasaki S Shima T Sugihara H Kunishige H Kuribayashi T Nakagawa M 《Japanese circulation journal》1999,63(5):333-338
To analyze the recent change in the long-term survival of patients with dilated cardiomyopathy (DCM), the present study comprised consecutive 111 patients with ejection fraction <50% and left ventricular end-diastolic diameter >58 mm. who were admitted to hospital from January 1983 to December 1994. The patients were divided into 2 groups: group A who were diagnosed before 1989 and group B diagnosed after 1990. Basic characteristics at diagnosis, including age, NYHA functional class, left ventricular end-diastolic diameter and ejection fraction, were similar between these 2 groups. Calculated survival rate at 5 years was 90.0% in group B in contrast to 62.3% in group A. Event-free survival also improved in group B. In group B, beta-blockers and angiotensin converting enzyme inhibitors were more frequently used than in group A (p<0.0001) whereas digitalis and other positive inotropic agents were significantly less used. Left ventricular ejection fraction was significantly improved during the follow-up period in patients treated with beta-blockers compared with those not treated with beta-blockers. These data indicate a significant improvement in the survival of patients with dilated cardiomyopathy after 1990, which may be explained by the change of medical treatment, especially the use of beta-blockers. 相似文献
88.
Kazuhiro Uda Kensuke Shoji Chitose Koyama-Wakai Munehiro Furuichi Noriyasu Iwase Seiichiro Fujisaki Shinji Watanabe Isao Miyairi 《Journal of infection and chemotherapy》2018,24(6):407-413
Background
Influenza A(H1N1)pdm09 virus infections often manifest severe respiratory symptoms, particularly in patients with a past history of allergic disease. Most of these findings were reported during the 2009 pandemic. The purpose of this study was to detail the clinical characteristics of influenza virus-induced lower respiratory infection (LRI) during the A(H1N1)pdm09-predominant 2015–2016 season.Methods
We retrospectively reviewed the clinical characteristics of influenza-induced LRI cases in children admitted to a tertiary children's hospital. Molecular diagnostic evaluation was performed on samples obtained from the most severe cases.Results
We identified 66 patients with influenza-associated hospitalization and included 21 patients with influenza virus-induced LRI for analyses. Twelve patients (57%) were admitted to the pediatric intensive care unit, seven (33%) required mechanical ventilation, and three (14%) required extracorporeal membrane oxygenation. Plastic bronchitis (PB) was identified in six patients (29%), among whom a past medical history of asthma or food allergy were noted in all six patients. A past history of allergic disease was more common among patients with, than among those without, PB (p = 0.009). A(H1N1)pdm09 was detected from all the PB cases, and phylogenetic analyses of the hemagglutinin and neuraminidase genes demonstrated that this virus belonged to subclades 6B.1 and 6B.2. In the six PB cases, we found one patient with H275Y mutation in neuraminidase.Conclusion
Allergic disease was a risk factor for developing PB due to influenza A(H1N1)pdm09 infection during the 2015–16 season. 相似文献89.
Mayumi Ishida Hideki Onishi Tatsuya Morita Yosuke Uchitomi Megumi Shimizu Satoru Tsuneto Yasuo Shima Mitsunori Miyashita 《Journal of pain and symptom management》2018,55(4):1061-1067.e1